miR-491 regulates glioma cells proliferation by targeting TRIM28 in vitro

Qi, Zengxin; Cai, Sanjun; Cai, Jiajun; Chen, Lingchao; Yu, Yao; Chen, Liang; Mao, Ying

doi:10.1186/s12883-016-0769-y

Cited by 31 publications

(29 citation statements)

References 25 publications

(33 reference statements)

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“…Accumulating evidence has revealed that miRNAs are crucial to brain physiology and tumorigenesis, especially in gliomas, where abnormally elevated levels of miR-10b, miR-21, and miR-93 and abnormally reduced levels of miR-101, miR-491, and miR-203 have been identified [12-14]. …”

Section: Introductionmentioning

confidence: 99%

Bufalin Inhibits Cellular Proliferation and Cancer Stem Cell-Like Phenotypes via Upregulation of MiR-203 in Glioma

Liu

Weng

et al. 2017

Cell Physiol Biochem

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Background/Aims: Prior studies have shown that bufalin inhibits cellular proliferation and induces apoptosis in various human cancers. MicroRNA-203 (miR-203) has been shown to function as an important regulator of tumor progression at various stages. In this study, we investigated the effect of miR-203 expression and bufalin treatment on glioma cell proliferation and stem cell-like phenotypes. Methods: We used cell viability assay, colony formation assay, cell apoptosis assay and neurosphere formation assay to dectect the treatment effect of bufalin on U251 and U87 cells. Cells were transfected with the miR-203 mimic without bufalin treatment or cells were transfected with anti-miR-203 under bufalin treatment, the above expreiments were repeated. RT-PCR was employed to quantify miR-203 expression. Western blot was performed to detect the stem cell-like (CSC) markers, OCT4 and SOX2. Luciferase activity assay was used to determine whether the SPARC is the target of miR-203. Results: Bufalin treatment inhibited cell proliferation, colony formation, and CSC phenotypes and increased cell apoptosis and expression of miR-203. Furthermore, overexpression of miR-203 led to similar outcomes as bufalin treatment with respect to the cell viability, colony formation, cell apoptosis and the phenotypes of glioma cells. While anti-miR-203 attenuated the inhibitory effects of bufalin as promoting cell proliferation, colony formation and CSC phenotyes and inhibiting cell apoptosis. In addition, we identified SPARC as a novel target gene of miR-203. Conclusions: These findings suggest that miR-203 plays an important role in bufalin’s ability to inhibit the growth of glioma cells and the development of stem cell-like phenotypes.

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Section: Introductionmentioning

confidence: 99%

Bufalin Inhibits Cellular Proliferation and Cancer Stem Cell-Like Phenotypes via Upregulation of MiR-203 in Glioma

Liu

Weng

et al. 2017

Cell Physiol Biochem

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“…High levels of TRIM28 correlated with a significantly lower survival rate in patients with ovarian, gastric and pancreatic cancer [10,16,27,28]. There was a positive correlation between TRIM28 expression and glioma malignancy [29,30]. Recently, it has been reported that TRIM28 could promote proliferation and metastatic progression in breast cancer cell [12].…”

Section: Discussionmentioning

confidence: 95%

TRIM28 is Overexpressed in Osteosarcoma and Associated with Tumor Progression

Cui¹,

Wang²,

Yang³

et al. 2017

Preprint

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Tripartite motif containing 28 (TRIM28) is a transcriptional co-factor with pleiotropic biological activities, especially in tumor cells. In this study, expression levels of TRIM28 in osteosarcoma (OS) tissues and the correlations with clinicopathological variables were investigated in 87 OS cases, meanwhile, cell and animal experiments were performed to detect the biological functions of TRIM28. The results showed that TRIM28 was overexpressed in OS tissues compared with normal bones, and TRIM28 expression correlated significantly with tumor diameter (χ2 = 4.06, p=0.04), metastasis (χ2 =11.10, p< 0.01) and clinical stage (χ2 =15.50, p< 0.01). Furthermore, patients with high TRIM28 level always had poor survival (p < 0.01). Functionally, TRIM28 knockdown significantly inhabited cell ability of proliferation and migration in OS cell lines of in vitro and in vivo experiments. Additionally, TRIM28 could significantly inhibited E-cadherin expression in reducing the stability of the TRIM28 mRNA. Therefore, TRIM28 overexpression was correlated with malignant progression of OS and poor survival of OS patients, and TRIM28 pathway may be a therapeutic target for OS.

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“…The counteractive effects of miRs against the expression of TRIM have been identified in various diseases, including the underexpression of TRIM32 in human immunodeficiency virus reduced by miR-155, underexpression of TRIM29 in gastric cancer by miR-185, as well as downregulated TRIM24 in gastric cancer by miR-511 [34-36]. A previous study has shown that miR-491 resulted in the suppression in the expression of TRIM28 in glioma cells by directly binding to the 3′-UTR of TRIM28 mRNA [37]. It was also found that the target relationship between miR-511 and TRIM24 might explain the downregulation in the expression of TRIM24 [36].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-653 Inhibits Thymocyte Proliferation and Induces Thymocyte Apoptosis in Mice with Autoimmune Myasthenia Gravis by Downregulating TRIM9

Cao

Dong²,

et al. 2019

Neuroimmunomodulation

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Objectives: Myasthenia gravis (MG) is an organ-specific autoimmune neuromuscular disorder that occurs as a result of the impairment in neuromuscular junction and autoantibody attack on the postsynaptic receptors. Increasing evidence suggests that microRNAs (miRs) might be involved in the development of MG. Therefore, the present study aimed to investigate the regulatory function of miR-653 on MG and its relationship with tripartite motif 9 (TRIM9). Methods: The thymic tissues obtained from MG patients with thymic hyperplasia were prepared for establishing an MG mouse model in BALB/c mice. Afterwards, the miR-653 and TRIM9 expressions were determined in thymic tissues. A dual-luciferase reporter assay was carried out to validate whether miR-653 directly targets TRIM9. Finally, the thymocytes were exposed to mimics or inhibitors of miR-653, or siRNA against TRIM9 with the use of MTT assays and flow cytometry for the verification of the gain or loss function of miR-653 and TRIM9 on viability, cell cycle progression, and apoptosis of thymocytes. Results: There was a decrease in thymocyte miR-653 and an increase in TRIM9 in thymic tissues of MG mice. miR-653 was found to negatively regulate TRIM9. Overexpression of miR-653 or depletion of TRIM9 resulted in the inhibition of cell viability, suppression of cell cycle progression, and induction of apoptosis rate in thymocytes. Conclusion: The findings from the present study provided evidence that miR-653 impairs proliferation and promotes apoptosis of thymocytes of MG mice by suppressing TRIM9, indicating that miR-653 could be used as potential therapeutic target in the treatment of autoimmune MG.

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miR-491 regulates glioma cells proliferation by targeting TRIM28 in vitro

Cited by 31 publications

References 25 publications

Bufalin Inhibits Cellular Proliferation and Cancer Stem Cell-Like Phenotypes via Upregulation of MiR-203 in Glioma

Bufalin Inhibits Cellular Proliferation and Cancer Stem Cell-Like Phenotypes via Upregulation of MiR-203 in Glioma

TRIM28 is Overexpressed in Osteosarcoma and Associated with Tumor Progression

MicroRNA-653 Inhibits Thymocyte Proliferation and Induces Thymocyte Apoptosis in Mice with Autoimmune Myasthenia Gravis by Downregulating TRIM9

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